Public Defence: Marc McGowan - Lung cancer drug resistance
M.Phil. Marc Kevin McGowan at Institute of Clinical Medicine will be defending the thesis “Drug-Resistance and Protective Factors in NSCLC” for the degree of PhD.
Trial Lecture - time and place
- First opponent: Associate Professor Maria Planck, Division of Oncology and Pathology, Faculty of Medicine, Lund University, Sweden
- Second opponent: Associate Professor Thomas Berg, Department of Pathology, University Hospital of North Norway
- Chair of the committee: Professor Jürgen Geisler, Faculty of Medicine, University of Oslo and Department of Oncology, Akershus University Hospital
Chair of the Defence
Associate Professor Lars Fjellbirkeland, Faculty of Medicine, University of Oslo
Associate Professor Odd Terje Brustugun, Oslo University Hospital
Lung cancer remains the most common cause of cancer-related deaths globally. The work in this thesis demonstrated the need for further research into new targets for drug development and highlights why some patients with early stage lung cancers have a favourable treatment outcome than others.
The aims of this thesis were to identify why some early stage lung cancer patients respond better to treatment than others. Further work included identifying drug-resistance in advanced stage lung cancers and determining if these new targets were of therapeutic value.
Usually, patients harbouring mutations in their genes will have a poor response to therapy. In our data we found that a protein responsible for cell survival was mutated in patients that received surgery and had a better survival than those without. This data is important for identifying patients whom may not require further treatment and also provide comfort at diagnosis.
Advanced stage lung cancers are much harder to treat with little therapeutic options. Using cell lines in culture we identified two new targets that may benefit from drug development. By generating cell lines to become resistant to drugs, we were able to identify new mechanisms of drug resistance. By silencing these genes, and reintroducing the same drugs, the cells all responded and died.
These results further our understanding of the disease and offer promising targets for drug development in the future.
Contact the research support staff.